2012 Fiscal Year Final Research Report
Analysis for mechanisms of neurotransmitter transport via Dysbindin
Project/Area Number |
23790291
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
General pharmacology
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Research Institution | Nagoya University |
Principal Investigator |
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Project Period (FY) |
2011 – 2012
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Keywords | 精神神経疾患 / 統合失調症 / 脆弱性遺伝子 |
Research Abstract |
Although the etiological mechanisms of psychiatric disorders, such as schizophrenia, remain largely esoteric, multiple hypotheses (e.g. dysfunction of dopamine, glutamate or serotonin, neurodevelopmental disorders, stress during pregnancy and viral infection) have been proposed. The dissection of molecular pathways centered on promising risk factors, such as Disrupted-In-Schizophrenia 1 (DISC1), may help us achieve a better understanding of the pathogenesis of these disorders. In this study, I identified a novel interacting protein complex, V-ATPase, as a partner of DISC1. I found significant protein reduction of a couple of V-ATPase subunits in synaptic vesicle fractions isolated from the DISC1-deficient mice compare to proteins isolated from the wildtype mice.
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[Journal Article] Behavioral alterations associated with targeted disruption of exons 2 and 3 of the DISC1 gene in the mouse2011
Author(s)
Kuroda K, Yamada S, Tanaka M, Iizuka M, Yano H, Mori D, Tsuboi D, Nishioka T, Namba T, Iizuka Y, Kubota S, Nagai T, Ibi D, Wang R, Enomoto A, Isotani-Sakakibara M, Asai N, Kimura K, Kiyonari H, Abe T, Mizoguchi A, Sokabe M, Takahashi M, Yamada K, and Kaibuchi K
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Journal Title
Hum. Mol. Genet
Volume: 20(23)
Pages: 4666-4683
DOI
Peer Reviewed
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